Congenital adrenal hyperplasia is also known as adrenogenital syndrome or adrenal perversion. It is mainly due to the defect of the enzymes necessary for the biosynthesis of adrenal cortical hormones, resulting in abnormal synthesis of cortical hormones. In most cases, the adrenal glands secrete insufficient glucose-regulating hormones and salt-regulating hormones, but excessive male hormones. Therefore, clinically, there are varying degrees of adrenal cortical hypofunction, accompanied by masculinization in girls and precocious puberty in boys. In addition, there may be various syndromes such as hyponatremia or hypertension. According to the type of defective enzyme, it can be divided into 5 categories: ①2l-hydroxylase (CYP21) deficiency, which is divided into typical salt-losing type, masculinizing type and atypical type; ②11β-hydroxylase (CYP11β) deficiency, which can be divided into type I and II; ③3β-hydroxysteroid dehydrogenase (3β-HSD) deficiency; ④17α-hydroxylase (CYP17) deficiency, with or without 17,20-chain cleavage enzyme (17,20LD) deficiency; ⑤cholesterol carboxylase deficiency. Clinically, 21-hydroxylase deficiency is the most common, accounting for more than 90%, with an incidence of about 1/4500 newborns, of which about 75% are salt-losing type, followed by β-hydroxylase deficiency, accounting for about 5% to 8%, with an incidence of about 1/5000 to 7000 newborns. Other types are rare.